Experimental inflammation was induced by injection of a suspension of kaolin in carboxymethylcellulose solution into a subcutaneous air pouch preformed on the back of rats. Endogenous bradykinin generated in the inflammatory pouch declined quickly unless kininase inhibitors were administered into the pouch. Bradykinin injected into the pouch brought about no significant increase in plasma exudation in the pouch unless kininase inhibitors were administered simultaneously. Although kininase I and II activities were present in normal rat serum, kininase II rather than kininase I was mainly responsible for the degradation of bradykinin in rat serum. In the pouch challenged with the kaolin suspension and vehicle, kininase II originating from the pouch wall tissue played a predominant role in the degradation of bradykinin while the role of kininases derived from the blood and inflammatory cells was minor.